Prof. Daniel M. Michaelson
Ph.D.: University of California, Berkeley, 1974
Phone: (Tel) +972-3-640-9624
(Fax) +972-3-640-7643
E-mail: dmichael@post.tau.ac.il
Room#: Sherman, 705
Member's portrait

Research Interests

Research Field

Alzheimer’s disease, neurodegeneration, apolipoprotein E, b-amyloid, brain inflammation, animal models

  

Research Activity

Alzheimer’s disease is the commonest of the dementias and it is thus of immense importance to unravel the mechanisms underlying brain dysfunction in this disease. Neurodegeneration in Alzheimer’s disease is associated with alterations in the expression and life cycle of several key molecules. These include the amyloid precursor gene, the presenilins PS1 and PS2, the allele E4 of apolipoprotein E (apoE) and the cytoskeletal protein tau. In addition, Alzheimer’s disease is associated with chronic brain inflammation .

  

The research in our group focuses on apolipoprotein E4 (apoE4), which is the most prevalent genetic risk factor of familial and sporadic Alzheimer’s disease, and on the role of cross talk interactions between apoE4 and other genetic and environmental risk factors of Alzheimer’s disease. This is pursued utilizing mice transgenic for apoE4 and apoE3, which is the benign apoE allele, and corresponding in vitro systems in experiments directed at the following problems :

  • Isoform specific effects of apoE4 on the aggregation, deposition and toxicity of b-amyloid in vivo .
  • The effects of environmental stimulation on the phenotypic expression of the apoE genotype .
  • The role of cross talk between apoE and brain inflammation in mediating the pathological effects of apoE4 .

Selected Publications
  1. Genis, I., Shohami, E. and Michaelson, D.M. (2000) Tau hyperphosphorylation in control and apoE-deficient mice following head injury.J. Neurosc. Res. 60: 559-564.
  2.  Chapman, S., Sabo, T., Roses, A.D. and Michaelson, D.M. (2000) Reversal of presynaptic deficits of apolipoprotein E-deficient mice in human apolipoprotein E transgenic mice Neuroscience 97: 419-424.
  3. Sabo, T., Lomnitski, L., Nyska, A., Beni, S., Maronpot, R.R., Shohami, E., Roses, A.D. and Michaelson, D.M. (2000) The susceptibility of transgenic mice expressing human apolipoprotein E to closed head injury: The allele E3 is neuroprotective whereas E4 increases fatalities. Neuroscience 101: 879-884.
  4. Chapman, J., Vinokurov, S., Achiron, A., Karussis, D.M., Mitosek-Szewczyk, K., Birnbaum, M., Michaelson, D.M. and Korczyn, A.D. (2001) ApoE genotype is a major predictor of long term progression of disability in multiple sclerosis. Neurology 66: 312-316.
  5. Chapman, J., Korczyn, A.D., Karussis, D.M. and Michaelson, D.M. (20010) The effects of APOE genotype on age at onset and progression of neurodegenerative diseases.  Neurology 57: 1482-1485.
  6. Ezra, Y., Oron, L., Roses, A.D., Beni, s.., Shohami, E. and Michaelson, D.M. (2003) Aplipoprotein E4 decreases whereas apolipoprotein E3 increases the level of secreted amyloid precursor protein after closed head injury. Neuroscience 121: 315-325.
  7. Levy, O., Yakovlev, G. and Michaelson, D.M. (2003) Apolipoprotein E4 impairs hippocampal  plasticity and blocks environmental stimulation of memory. Neurobiology of Disease 13: 273-282.
  8. Ophir, G., Meilin, S., Efrati, M., Chapman, J., Karussis, D., Roses, A. and Michaelson, D.M. (2003) Human apoE3 but not apoE4 rescues impaired astrocyte activation in apoE null mice. Neurobiol. Dis. 12: 56-64.
  9. Ophir, G., Levi, O., Yakovlev, G. and Michaelson, D. (2004) The phenotypic effects of the apoE genotype in transgenic mice. Brain Aging 4: 29-33.
  10. Dolev, I. and Michaelson, D.M. (2004) A nontransgenic mouse model shows inducible amyloid-b (Ab) peptide deposition and elucidates the role of apolipoprotein E in the amyloid cascade. Proc. Natl. Acad. Sci. (USA) 101: 13909-13914.

Students and Lab Members

 

Belinson Haim

 

Dolev Iftach

 

Gilat Aya

Levi Ofir

Mizrahi Liza

 

Nisemblat Yotam

 

Ophir Gal

 

Dima

 

 

Keren Bornshtein

 

Aliza Dvir

 

 


Courses

1. THE MOLECULAR  MECHANISMS UNDERLYING ALZHEIMER'S DISEASE

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